Microscopic observation on morphological changes of basophils induced by cross-linking of IgE receptors
نویسندگان
چکیده
Differences in morphological changes of basophils between antigen and antiIgE stimulation were examined in atopic subjects in relation to histamine release. 1. Antigen-induced release of histamine was remarkably more rapid and larger at any incubation time than the release by anit-lgE. and a significant difference was found at 3 to 9 min. 2. Decrease in number of basophils induced by antigen was significantly higher for 12 to 15 min incubation time than that by anti-lgE. 3. Morphological changes of basophils representing increased motility such as an increased ratio of short to long axis diameter (L/S ratio) and an increased incidence of basophils with localized granules (LG) were more often observed in antigen stimulation compared with anti-lgE. and the L/S ratio of the cells was significantly more increased in antigen stimulation at 6 and 15 min. 4. There was no difference in morphological changes of basophils showimg swollen type (degranulation) such as an increased mean diameter (MD) of the cells between antigen and anti-lgE. These results suggest that antigen activates basophils and induces increased motility more strongly than anti-lgE. but the action on degranulation was not different between the two agents.
منابع مشابه
Alternative Anaphylactic Routes: The Potential Role of Macrophages
Anaphylaxis is an acute, life-threatening, multisystem syndrome resulting from the sudden release of mediators from effector cells. There are two potential pathways for anaphylaxis. The first one, IgE-dependent anaphylaxis, is induced by antigen (Ag) cross-linking of Ag-specific IgE bound to the high-affinity IgE receptor (FcεRI) on mast cells and basophils. The second one, IgG-dependent anaphy...
متن کاملRegulation of high-affinity IgE receptor-mediated mast cell activation by murine low-affinity IgG receptors.
Allergic symptoms result from the release of granular and lipidic mediators and of cytokines by inflammatory cells. The whole process is initiated by the aggregation of mast cell and basophil high-affinity IgE receptors (Fc epsilon RI) by IgE and antigen. We report here that IgE-induced release of mediator and cytokine can be inhibited by cross-linking Fc epsilon RI to low-affinity IgG receptor...
متن کاملMast cells and basophils are selectively activated in vitro and in vivo through CD200R3 in an IgE-independent manner.
Mast cells and basophils have been implicated in the host defense system against pathogens and in the development of allergic disorders. Although IgE-dependent responses via FcepsilonRI on these cells have been extensively studied, little is known about cell surface molecules that are selectively expressed by these cells and engaged in their activation via an IgE-independent mechanism. We have ...
متن کاملHistamine release from the basophils of control and asthmatic subjects and a comparison of gene expression between "releaser" and "nonreleaser" basophils.
Most human blood basophils respond to FcepsilonRI cross-linking by releasing histamine and other inflammatory mediators. Basophils that do not degranulate after anti-IgE challenge, known as "nonreleaser" basophils, characteristically have no or barely detectable levels of the Syk tyrosine kinase. The true incidence of the nonreleaser phenotype, its relationship (if any) to allergic asthma, and ...
متن کاملIgE-independent interleukin-4 expression and induction of a late phase of leukotriene C4 formation in human blood basophils.
T-helper cells can differentiate into at least two subtypes secreting distinct profiles of cytokines, Th1 and Th2, regulating immunoprotection and different immunopathologies. Interleukin-4 (IL-4) is both the product and the inducer of Th2 cells, raising the question whether IL-4 can be produced in response to antigen-independent stimuli. Here we show that human basophils produce IL-4 on stimul...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2009